Submitted to: Journal of Insect Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: August 27, 2005
Publication Date: December 31, 2005
Citation: Gelman, D.B., Gerling, D., Blackburn, M.B. 2005. Host-parasite interactions relating to penetration of bemisia tabaci by its parasitoid eretmocerus mundus. Journal of Insect Science. 5(46).
Interpretive Summary: The sweet potato whitefly attacks more than 600 different kinds of plants in both field and greenhouse settings, and causes billions of dollars of damage in crop losses each year, world-wide. These tiny insects damage plants by feeding on plant juices, transmitting pathogenic viruses and producing honeydew, a sweet sticky substance that supports the growth of mold. For the last several decades, chemical pesticides have been the preferred method for controlling pest species of whiteflies. Tiny wasp parasites in addition to being useful as biological control agents could contribute to the development of new biopesticides (compounds that would kill insects without harming other living things), if only the complex mechanisms by which they manipulate their host insect's life processes were well-understood. Unfortunately, there is very little information available in this area of research. Here we describe signals provided by the host insect that are required for the parasite, Eretmocerus mundus, to grow and develop as well as mechanisms used by the parasite to control whitefly development. Our results show that: 1) parasite egg laying and penetration into the whitefly is cued by the age and stage of the whitefly host, 2) the parasite delivers substances that cause whitefly cells to multiply and form a protective capsule that engulfs the parasite as it enters the whitefly, that reduce whitefly molting hormone titers, and that prevent the whitefly from completing its development. Results should be useful to other scientists, and should help to identify compounds that would contribute to the production of biopesticides.
Eretmocerus mundus, parasitizes all four nymphal instars of the sweet potato whitefly, with 3rd instars being the preferred hosts. Eggs are laid underneath the host nymph. First instars hatch and later penetrate the whitefly. It is known that the initiation of parasitoid penetration induces the host to form a cellular capsule around the parasitoid. We have determined that females never oviposit once the 4th instar whitefly nymph has undergone adult development. Upon hatch (occurred under 2nd-4th instar nymphs), only the larval mouthparts protruded through the chorion and were in contact with the external environment. Parasitoid penetration and the concomitant shedding of the remaining chorion did not occur until the host whitefly had reached the 4th instar. The non-penetrating E. mundus larva almost always induced permanent developmental arrest in its host whitefly and caused a reduction in host ecdysteroid titers. Therefore, unless there is a localized peak (near the site of penetration), it appears that the induction of capsule formation does not depend upon an increase in ecdysteroid levels. As the capsule formed around the penetrating parasitoid, host epidermal cells, in the area of penetration, multiplied and became columnar, and new cuticle was deposited within the developing capsule. This cuticle was thick in the ventral portion of the capsule, thinner in the dorsal part and appeared to be absent at its apex. Our results provide important new information regarding the timing of parasitoid oviposition and egg hatch as related to larval penetration, and concerning parasitoid-induced changes in whitefly development, molting hormone titers and the process of capsule formation.